Evidence map›Paper›PMID 42714250›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2026

Loss of Vacuole Membrane Protein 1 protects against acetaminophen-induced liver injury by modulating inflammation and hepatocyte proliferation.

Khue Nguyen, Mengwei Niu, Hong-Min Ni

Abstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Khue NguyenDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, United States.
Mengwei NiuDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, United States.
Hong-Min NiDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, United States.ORCID 0000-0002-5300-2654

Funding

longitudinal assessment of stress and stress-related concepts across a behavioral weight loss interventionP20GM144269 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI John P Thyfault, STEVEN A WEINMAN · 2022 to 2026
$14.9M
Novel mechanisms regulating VLDL secretion and non-alcoholic fatty liver diseasesR56DK129234 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NI, HONGMIN · 2021 to 2021
$402k
National Institute of General Medical Sciences of Centers of Biomedical Research Excellence (COBRE) P20GM144269NIDDK NIH HHS DK129234NIDDK NIH HHS R56 DK129234NIGMS NIH HHS P20 GM144269
6 · The paper itself

Abstract

Acetaminophen (APAP) overdose is a leading cause of severe liver injury and acute liver failure (ALF). Increased hepatic macrophages promote inflammation and clear necrotic cell debris, thereby promoting a regenerative state for liver repair during APAP-induced liver injury. Vacuole membrane protein 1 (VMP1) is an ER transmembrane protein essential for autophagy. Deletion of VMP1 in the liver impairs autophagy. The role of VMP1 in APAP-induced liver injury is unknown. In this study, the human APAP ALF RNA sequencing database was analyzed. Liver-specific Vmp1 knockout (Vmp1LKO) and matched wild-type (Vmp1LWT) mice were administered 500 mg/kg APAP. Liver injury, necrosis, and other biochemical analyses were assessed. Increased mRNA levels of VMP1 and autophagy-related genes were found in human APAP ALF livers. Serum ALT and hepatic necrosis were increased in WT mice following APAP treatment. LC3B-II and p62 were increased, but VMP1 protein decreased in WT mouse livers following APAP treatment. Liver injury was markedly decreased in Vmp1LKO mice compared with their WT littermates. Basal hepatic CYP2E1 and glutathione (GSH) levels were similar between genotypes, but increased lipid-laden macrophages (foam cells) were present in Vmp1LKO livers. Interestingly, APAP protein adduct formation decreased in Vmp1LKO mouse livers, but mitochondrial damage was similar in both phenotypes. Peroxynitrite formation was observed in APAP-treated Vmp1LWT hepatocytes but was limited in foam cells of Vmp1LKO mouse livers. Furthermore, GSH replenishment and liver regeneration were enhanced in Vmp1LKO mouse livers. In conclusion, loss of hepatic VMP1 protects against APAP-induced liver injury by replenishing GSH, modulating inflammation, and enhancing liver regeneration.

Indexed as

AcetaminophenCell ProliferationChemical and Drug Induced Liver InjuryHepatocytesMembrane ProteinsAnimalsAutophagyHumansInflammationLiverMaleMiceMice, Inbred C57BLMice, KnockoutAcetaminophenMembrane ProteinsVMP1 protein, humanautophagyglutathioneliver regenerationmitochondrianecrosis

Identifiers

PMID42714250
PMCPMC13614422

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.